EXTRACT & BLOT HtrA1 maxi
- Known as:
- EXTRACT & BLOT HtrA1 maxi
- Catalog number:
- 30501004
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- BioTeZ
- Gene target:
- EXTRACT & BLOT HtrA1 maxi
Related genes to: EXTRACT & BLOT HtrA1 maxi
- Gene:
- HTRA1 NIH gene
- Name:
- HtrA serine peptidase 1
- Previous symbol:
- PRSS11
- Synonyms:
- HtrA, IGFBP5-protease, ARMD7
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2016-10-05
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*Pentachloro Rose Bengal Yeast Extract Agar Base (PRYES Agar) USE For the cultivation and differentiation of nephrotoxin producing strains of Penicillium viridicatum and related species isolated f*Pentachloro Rose Bengal Yeast Extract Agar Base (PRYES Agar) USE For the cultivation and differentiation of nephrotoxin producing strains of Penicillium viridicatum and related species isolated f1 X PBS with 0.05% Sodium Azide,, Western Blot Analysis10 X MOPS Buffer, Southern_Nothern Blot analysis10X PBS with 0.5% Tween 20, pH 7.4., Western Blot Analysis10X TBS with Tween-20 V3, Western Blot Analysis10X TBS with Tween-20, Western Blot Analysis10X TBS with Tween-20, Western Blot Analysis10X TBS, Western Blot Analysis10X TBS, Western Blot Analysis10X Tris-Glycine Buffer(w_o SDS), Western Blot Analysis10x Washing buffer, pH 7.5, Western Blot Analysis10x Western transfer buffer, carbonate, Western Blot Analysis1st Strand cDNA Maxi Archive System1st Strand cDNA Maxi Archive System Related articles to: EXTRACT & BLOT HtrA1 maxi
- Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss worldwide and is characterized by substantial clinical, imaging, and molecular heterogeneity that complicates disease prediction and therapeutic management. Recent advances in artificial intelligence (AI) and precision therapeutics have created new opportunities for more individualized and data-driven AMD care. AI models trained on multimodal datasets-including fundus photography, optical coherence tomography (OCT), optical coherence tomography angiography (OCTA), genetic susceptibility loci (e.g., CFH, ARMS2/HTRA1, C3, CFI, and APOE), and longitudinal clinical information-have demonstrated promising capability in early disease detection, progression forecasting, biomarker identification, and prediction of treatment response. These developments align closely with emerging precision therapeutic strategies, including optimized anti-vascular endothelial growth factor (anti-VEGF) regimens, complement-targeted therapies, gene-based interventions, and stem cell-associated regenerative approaches. This review provides a translational overview of AI-enabled precision therapeutics in AMD, with emphasis on multimodal biomarker integration, individualized therapeutic stratification, longitudinal disease monitoring, and clinically interpretable AI systems. Importantly, we further propose a Five-Level Clinical Readiness and Translational Utility Framework for AI in AMD Precision Therapeutics, categorizing AI applications according to evidence strength, clinical maturity, validation status, interpretability, and real-world implementation potential. The framework distinguishes near-reference-standard imaging AI systems, advanced clinical decision-support tools, emerging multimodal precision therapeutic AI, supportive workflow-oriented AI systems, and currently limited or unsuitable AI applications. Despite substantial progress, important translational barriers remain, including limited external validation, retrospective study designs, dataset heterogeneity, domain shift, insufficient explainability, regulatory uncertainty, and challenges related to workflow integration and real-world clinical deployment. Future advances in multimodal longitudinal AI, explainable AI, federated learning, digital health platforms, and multi-omics integration may facilitate a transition from reactive disease management toward more proactive, predictive, and personalized ophthalmic care. Collectively, AI-enabled precision therapeutics may help establish a more scalable and clinically integrated framework for individualized AMD management and future precision ophthalmology. - Source: PubMed
Publication date: 2026/08/17
Wang Mini HanLee Simon Ming YuenWang YapengAlves José CXie RuitaoHe YaqingHou GuanghuiFang XiaoxiaoYu YangCai XiaodongZheng ShuaiLiu JinCheang ChoninKuok Kai IanQin Shuai - Cerebral small vessel disease (CSVD) describes a range of neurological diseases affecting the small arteries, veins, and capillaries which supply the white matter and deep grey matter structures of the brain. They are the most common form of cerebrovascular disease, accounting for almost half of vascular dementia cases and approximately 20% of stroke incidence globally. Genetic testing is a routine diagnostic tool for monogenic CSVDs; however, less than 20% of patients have a causal variant in a known gene. Genetic testing for these disorders focuses on single nucleotide variants and short insertions or deletions, with larger genomic variation often unexplored as a cause of disease. In this study we performed whole-exome sequencing (WES) on 111 patients suspected of familial CSVD that had previously tested negative for pathogenic variants in seven known CSVD genes (NOTCH3, HTRA1, COL4A1, COL4A2, TREX1, GLA, and FOXC1). Bioinformatic analysis of WES data, multiplex ligation-dependent probe amplification, quantitative real-time polymerase chain reaction assays, and Nanopore long-read sequencing were used to identify suspected copy number variants. This work identified four candidate CNVs across NOTCH3, LMNB1, and COL4A2 which are potential causes of CSVD and highlights the need for further investigation of more complex forms of genetic variation and their potential roles as causal of CSVD. - Source: PubMed
Publication date: 2026/08/27
Guyler Solomon KMaksemous NevenLea Rodney ASmith Robert ASutherland Heidi GGriffiths Lyn R - A peripheral nerve sheath tumour composed predominantly of Wagner-Meissner (W-M) bodies is typically regarded as a variant of schwannoma and has been considered rare. Interestingly, a SH3PXD2A::HTRA1 fusion was found which is described in schwannomas with a so-called "serpentine" palisading pattern comprising short palisades of Schwann cells. - Source: PubMed
Publication date: 2026/08/26
Wilsher Mark JamesBerber Onur - The vascular system is the largest organ in the body and underlies most chronic diseases, yet the molecular mechanisms that govern its plasticity remain poorly defined. - Source: PubMed
Publication date: 2026/08/13
Amrute Junedh MJiang LihuaBolar NikhitaHiga KellyZhu ChenchenJian RuiqiKim JenniferDuda MatthewPuaala Anna MarieKlinder AvaniDalal AlexPedroza AlbertReinhardt Dieter PCheng PaulSnyder MichaelFischbein Michael P - Age-related macular degeneration (AMD) is a complex disease wherein age, genetics, and environment play a role. How each of these factors contribute to the overall disease initiation and progression remains largely unelucidated. A renewed examination of the existing literature regarding the blood supply to the outer retina may provide novel insights. Hypoxia in the retinal pigment epithelium (RPE) can produce features of AMD, including photoreceptor degeneration. In the macula, the choriocapillaris has unique features making it susceptible to hypoperfusion, producing low-grade ischemia and chronic tissue hypoxia. The choriocapillaris experiences vascular loss and decreased blood flow early in AMD. Genetic risk, when viewed through a new lens, points to vascular insult as central to AMD pathophysiology. Complement-related risk genes are active in the vasculature, from large tributary vessels to small vessels of the choriocapillaris. HtrA serine peptidase 1 (HTRA1) is associated with cerebral small vessel disease and localizes to the choriocapillaris in AMD. Ageing can be interpreted as inevitable atherosclerosis from large to small vessels of the cerebral system. Western diets, smoking, and a rising prevalence of metabolic syndrome in people over age 60 are confirmed to accelerate both atherosclerosis and AMD. A perfusion-based model for complement-related, soft drusen-associated AMD is proposed while also explaining a second phenotype of non-complement related subretinal drusenoid deposit-associated AMD. Common to both phenotypes of AMD is chronic hypoperfusion causing decreased oxygen exchange and waste removal at the neurovascular unit of the choriocapillaris, RPE, and photoreceptors. Understanding AMD as an end-organ vascular disease may move us towards a unifying hypothesis. - Source: PubMed
Publication date: 2026/08/05
Holekamp Nancy MIvanova Simona Ivanova